Share on Facebook Share LinkedIn Pinterest Share on Twitter Email Scientists at the University at Buffalo have identified the mechanisms behind a genetic mutation that produces certain autistic behaviors in mice, as well as therapeutic strategies to restore normal behaviors.The research describes the cellular and molecular basis behind some autistic behaviors; it also suggests potential biomarkers and pharmaceutical targets.Published May 28 in Cell Reports, the research was led by Zhen Yan, PhD, professor in the Department of Physiology and Biophysics in the UB School of Medicine and Biomedical Sciences. The paper focuses on the loss of a gene called Shank3, an important risk factor for autism spectrum disorders (ASD). The researchers trace how this risk factor disrupts communication between neurons, leading to social deficits in mice. And, in their most important finding, they are able to reverse these neuronal disruptions, restoring normal behavior in mice.Previous studies have shown that approximately 84 percent of people with a Shank3 deletion or loss-of-function mutation had an ASD. But just how this occurs has remained unknown.The paper states that mice with a Shank3 deficiency exhibited “drastically reduced” interest in social stimuli, i.e., other mice, versus inanimate objects, suggesting “severe social deficits.” They also spent significantly more time in repetitive self-grooming than normal mice.The UB researchers found that the Shank3 deficiency plays a key role in how neurons communicate. It has a significant effect on the activation of the NMDA (n-methyl-D-aspartate) receptor, which is critical to learning and memory.Yan explained that the Shank3 deficiency disrupts the trafficking of this receptor and its function at critical transmission sites in the brain. That disruption, they found, results from the dysregulation of actin filaments, which act as a kind of cellular “highway” in the brain’s prefrontal cortex, the command center for “high-level” executive functions and a key region implicated in ASD.“This research is the first to show that, in animals, abnormal actin regulation causes autism-like behaviors,” said Yan.“Actin filaments are very dynamic structures that are constantly being assembled and disassembled, processes controlled by numerous regulators,” Yan explained.When something upsets the equilibrium of actin filament assembly, key cellular functions fall apart.“With Shank3 deficiency, we have found that the expression or activity of some actin regulators, such as cofilin, is altered,” explained Yan. “This upsets the equilibrium of actin filament assembly, which, in turn, disrupts the normal delivery and maintenance of NMDA and other critical receptors.”The result is a very significant effect on the functional plasticity of the synapse, which, in turn, leads to the manifestation of some autistic behaviors.In its most dramatic finding, the researchers found they were able to reverse this process, restoring normal behaviors in the Shank3-deficient mice, once the activity of cofilin or other regulators was returned to normal. This, in turn, restored actin dynamics at cortical synapses, allowing for the normal trafficking and functioning of NMDA receptors.“Once actin filaments and NMDA receptors returned to normal, we observed a robust and long-lasting rescue of the social interaction deficits and repetitive behavior in the Shank3-deficient mice,” said Yan. “Our results suggest a promising therapeutic strategy for treating autism.”The researchers are seeking funding to continue their work developing potential biomarkers and treatments for autism.
Email Share on Twitter Share on Facebook LinkedIn Children with even mild or passing bouts of depression, anxiety and/or behavioral issues were more inclined to have serious problems that complicated their ability to lead successful lives as adults, according to research from Duke Medicine.Reporting in the July 15 issue of JAMA Psychiatry, the Duke researchers found that children who had either a diagnosed psychiatric condition or a milder form that didn’t meet the full diagnostic criteria were six times more likely than those who had no psychiatric issues to have difficulties in adulthood, including criminal charges, addictions, early pregnancies, education failures, residential instability and problems getting or keeping a job.“When it comes to key psychiatric problems — depression, anxiety, behavior disorders — there are successful interventions and prevention programs,” said lead author William Copeland, Ph.D., assistant clinical professor of Psychiatry and Behavioral Sciences at Duke. “So we do have the tools to address these, but they aren’t implemented widely. The burden is then later seen in adulthood, when these problems become costly public health and social issues.” Share Pinterest Copeland and colleagues analyzed data from the Great Smoky Mountains Study, which began nearly two decades ago and includes 1,420 participants from 11 North Carolina counties. The study is ongoing and has followed the participants from childhood through adulthood — most are now in their 30s.Among the study group, 26.2 percent met the criteria for depression, anxiety or a behavioral disorder in childhood; 31 percent had milder forms that were below the full threshold of a diagnosis; and 42.7 percent had no identified problems.The researchers found that as these children grew into adults, even some of those who had no psychiatric diagnosis as children — nearly one in five — stumbled in adulthood, suggesting that difficulties were not limited to those with psychiatric diagnoses.But having a psychiatric diagnosis or a close call dramatically raised the odds that adulthood would have rough patches. This was the case even if they did not continue to have psychiatric problems in adulthood.Of those with the milder psychiatric indicators as kids, 41.9 percent had at least one of the problems in adulthood that complicates success, and 23.2 percent had more than one such issue. For those who met the full psychiatric diagnosis criteria, 59.5 percent had a serious challenge as adults, and 34.2 percent had multiple problems.Copeland said specific psychiatric disorders were associated with specific adult problems, but the best predictor of having adult issues was having multiple psychiatric problems as kids.“When we went into this, it was an open question: Are these psychiatric diagnoses in childhood impairing in the moment, but something people recover from and go on?” Copeland said. “We weren’t expecting to find these protracted difficulties into adulthood.”Copeland said the findings reinforce the need to attack problems early with effective therapies. He said only about 40 percent of children get the treatment they need for psychiatric disorders, and even fewer who have borderline problems are treated.“A big problem with mental health in the United States is that most children don’t get treatment and those who do don’t get what we would consider optimal care,” Copeland said. “So the problems go on much longer than they need to and cost much more than they should in both money and damaged lives.”
“This is not by any means the device that you’re going to implant into a patient,” said Karumbaiah, an assistant professor of animal and dairy science in the UGA College of Agricultural and Environmental Sciences. “This is proof of concept that extracellular matrix can be used to ensheathe a functioning electrode without the use of any other foreign or synthetic materials.”Implantable neural prosthetic devices in the brain have been around for almost two decades, helping people living with limb loss and spinal cord injury become more independent. However, not only do neural prosthetic devices suffer from immune-system rejection, but most are believed to eventually fail because of a mismatch between the soft brain tissue and the rigid devices.The collaboration, led by Wen Shen and Mark Allen of the University of Pennsylvania, found that the extracellular matrix derived electrodes adapted to the mechanical properties of brain tissue and were capable of acquiring neural recordings from the brain cortex.“Neural interface technology is literally mind boggling, considering that one might someday control a prosthetic limb with one’s own thoughts,” Karumbaiah said.The study’s joint collaborators were Ravi Bellamkonda, who conceived the new approach and is chair of the Wallace H. Coulter Department of Biomedical Engineering at the Georgia Institute of Technology and Emory University, as well as Allen, who at the time was director of the Institute for Electronics and Nanotechnology.“Hopefully, once we converge upon the nanofabrication techniques that would enable these to be clinically translational, this same methodology could then be applied in getting these extracellular matrix derived electrodes to be the next wave of brain implants,” Karumbaiah said.Currently, one out of every 190 Americans is living with limb loss, according to the National Institutes of Health. There is a significant burden in cost of care and quality of life for people suffering from this disability.The research team is one part of many in the prosthesis industry, which includes those who design the robotics for the artificial limbs, others who make the neural prosthetic devices and developers who design the software that decodes the neural signal.“What neural prosthetic devices do is communicate seamlessly to an external prosthesis,” Karumbaiah said, “providing independence of function without having to have a person or a facility dedicated to their care.”Karumbaiah hopes further collaboration will allow them to make positive changes in the industry, saying that, “it’s the researcher-to-industry kind of conversation that now needs to take place, where companies need to come in and ask: ‘What have you learned? How are the devices deficient, and how can we make them better?’” Share Share on Twitter Pinterest Share on Facebook Email LinkedIn Recent research published in the journal Microsystems & Nanoengineering could eventually change the way people living with prosthetics and spinal cord injury lead their lives.Instead of using neural prosthetic devices–which suffer from immune-system rejection and are believed to fail due to a material and mechanical mismatch–a multi-institutional team, including Lohitash Karumbaiah of the University of Georgia’s Regenerative Bioscience Center, has developed a brain-friendly extracellular matrix environment of neuronal cells that contain very little foreign material. These by-design electrodes are shielded by a covering that the brain recognizes as part of its own composition.Although once believed to be devoid of immune cells and therefore of immune responses, the brain is now recognized to have its own immune system that protects it against foreign invaders.
Email Share on Facebook LinkedIn Pinterest Share on Twitter In real estate, location is key. It now seems the same concept holds true when it comes to stopping pain.New research at Washington University School of Medicine in St. Louis and McGill University in Montreal indicates that the location of receptors that transmit pain signals IS important in how big or small a pain signal will be and how effectively drugs can block those signals.Blocking pain receptors in the nucleus of spinal nerve cells could control pain more effectively than interfering with the same type of receptors located on cell surfaces, the research shows. The scientists also found that when those same nerve cells encounter a painful stimulus, some of the receptors migrate from the cell surface into the nucleus. “Chronic pain affects almost 30 percent of Americans, and we’ve found, in rats, that by blocking specific receptors inside the cell, we can block pain,” said co-senior author Karen O’Malley, PhD, a professor of neuroscience at Washington University. “If we can find ways to specifically block pain receptors inside of cells rather than on the cell surface, we may make a big dent in chronic pain with fewer drug-induced side effects.”The study is published online Feb. 3 in the journal Nature Communications.The researchers focused on a specific type of glutamate receptor that is part of the family of receptors called G-protein-coupled receptors, which are important in signaling between neurons.In a rat model that mimics a type of chronic, neuropathic pain, animals treated with investigational drugs to block the activity of the receptors in the nucleus responded in ways suggesting they had gotten relief from their pain.“Drugs that penetrate the spinal nerve cells to block receptors at the nucleus were effective at relieving neuropathic pain, but those that didn’t penetrate the cells were not,” said McGill’s Terence J. Coderre, PhD, who developed the rat model.Coderre also explained that rats with nerve injuries displayed less spontaneous pain and less hypersensitivity to a painful stimulus when those nuclear receptors were blocked. But normal rats without nerve injuries had no changes in pain sensitivity when those receptors were blocked and the animals were exposed to a painful stimulus.“This is the first time we’ve been able to demonstrate that receptors inside the cell, on the nucleus, affect behavior in living animals,” O’Malley said.Coderre quipped: “By engineering drugs to target glutamate receptors at the nucleus, I guess you could say that pain treatment has gone nuclear.”Scientists have been studying glutamate receptors in the pain pathway for decades. What’s new, O’Malley explained, is that these most recent experiments — in cell cultures and rats — demonstrate that the location of the receptor in the cell has a major effect on the cell’s ability to transmit pain signals.For example, the researchers found that when these particular glutamate receptors on the nucleus of a nerve cell were activated, the response — measured by the amount of calcium released– was nine times larger than when the same type of receptor was activated on the cell’s surface. Changes in calcium levels play a key role in signaling in neurons. Increased calcium can release important neurotransmitters, regulate specific genes and contribute to synaptic changes that are critical to pain signals.“The nuclear calcium response goes up and stays up for a significant period of time — about four minutes,” O’Malley said. “The increased levels of nuclear calcium activate pathways that carry pain signals from the nerves to the brain.”They also found that the glutamate receptors on the nucleus responded to painful stimuli more robustly than the same types of receptors located on the cell’s surface, and that when the cells encountered such a stimulus, some receptors migrated from the surface to the nucleus. The researchers also discovered that receptors located in the nucleus stopped activating pain signals when targeted with drugs.The researchers focused mainly on nerve cells in the spinal cord, an important area for transmitting pain signals coming from all parts of the body. Future research will be aimed at determining what events cause the glutamate receptors to migrate to the nucleus and how to make drugs that more specifically block only glutamate receptors in the nucleus of the nerve cells. Share
“No [previous] studies have tested whether ICB-WGA is more strongly related to substance use or disordered eating, which may have future implications for eating disorder and substance abuse research fields,” said Tyler K. Hunt, primary researcher on the project.The team assessed 579 college students at a large Midwestern University–53 percent of participants were women, and 47 percent were men. Participants took a series of assessments, listed below.Eating Pathology Symptoms Inventory (EPSI): This questionnaire is used to measure the extent to which participants have engaged in various eating-related behaviors within the last two weeks. It contains statements like “I skipped 2 meals in a row.”Alcohol Use Disorders Identification Test (AUDIT): This survey contains questions that assess disordered drinking behaviors. Some example questions are “How often during the last year have you found that you were not able to stop drinking once you started?” and “Have you or someone else been injured as a result of your drinking?”ICG-WGA questionnaire: This questionnaire, developed by the research team, includes five statements designed to assess how much participants have engaged in compensatory and binge-drinking behaviors within the last two weeks. Statements include “I skipped a meal in order to counteract the calories from alcohol.” and “I engaged in strenuous exercise to compensate for calories consumed during drinking.”The results determined that students who engaged in certain disordered eating behaviors were likely to also engage in ICB-WGA. The most common linked behaviors were skipping meals, binge eating, excessive exercise and purging. The results also showed a strong link between alcohol abuse and ICB-WGA, indicating that the behavior pattern shares properties of both types of disordered behaviors.Scientists found similar results between men and women–both sexes were likely to engage in disordered eating behaviors and binge drinking. Men were more likely to report engaging in binge eating under the influence of alcohol, while women were more likely to report skipping meals and excessive exercise.The results may have important implications for future research and treatment.“These individuals may be at-risk for future development of both full-threshold eating and substance disorders,” said Hunt.“Our findings highlight the need for future research to identify the potential long-term course and outcome of ICB-WGA and develop secondary prevention programs to reduce the likelihood of ICB-WGA developing into full-threshold eating and substance use disorders.” Email Share A new behavior trend may be linked to eating disorders and substance abuse disorders, scientists say.“Drunkorexia” is a behavior pattern of repeatedly fasting or purging to compensate for the amount of calories consumed during binge drinking. Also known as Inappropriate Compensatory Behavior to avoid Weight Gain from consuming Alcohol (ICB-WGA), the behavior has been observed on several college campuses.A new study in Eating Disorder Behaviors examined the link between ICB-WGA and other disordered behavior patterns. Researchers were also interested in determining whether gender plays a role in this link. The study is the first of its kind. LinkedIn Share on Twitter Share on Facebook Pinterest
Email LinkedIn Share on Facebook Pinterest Share Lead author Dr Yujiang Wang, of Newcastle University, explains: “One of the key features of a mammalian brain is the grooves and folds all over the surface — a bit like a walnut — but until now no-one has been able to measure this folding in a consistent way.“By mapping the brain folding of over 1,000 people, we have shown that our brains fold according to a simple universal law. We also show that a parameter of the law, which is interpreted as the tension on the inside of the cortex, decreases with age.“In Alzheimer’s disease, this effect is observed at an earlier age and is more pronounced. The next step will be to see if there is a way to use the changes in folding as an early indicator of disease.”Common in all mammalsThe expansion of the cerebral cortex is the most obvious feature of mammalian brain evolution and is generally accompanied by increasing degrees of folding of the cortical surface.In the average adult brain, for example, if the cortex of one side — or hemisphere — was unfolded and flattened out it would have a surface area of about 100,000 mm2, roughly one and a half times the size of a piece of A4 paper.Previous research has shown that folding of the cortex across mammalian species follows a universal law – that is, regardless of size and shape, they all fold in the same way.However, until now there has been no systematic study demonstrating that the same law holds within a species.Tension slackens with age“Our study has shown that we can use this same law to study changes in the human brain,” explains Dr Wang, based in Newcastle University’s world-leading School of Computing Science.“From this, we identified a parameter that decreases with age, which we interpret as changing the tension on the cortical surface. It would be similar to the skin. As we age, the tension drops and the skin starts to slacken.“It has long been known that the size and thickness of the cortex changes with age but the existence of a general law for folding shows us how to combine these quantities into a single measure of folding that can then be compared between genders, age groups and disease states.”Women’s brains less foldedThe team also found that male and female brains differ in size, surface area, and the degree of folding. Indeed, female brains tend to be slightly less folded than male brains of the same age. Despite this, male and female brains are shown to follow exactly the same law.“This indicates that for the first time, we have a consistent way of quantifying cortical folding in humans,” says Dr Wang.Throughout the lifespan of healthy individuals, cortical folding changes in the same way in both men and women but in those with Alzheimer’s disease the change in the brain folding was significantly different.She adds: “More work is needed in this area but it does suggest that the effect Alzheimer’s disease has on the folding of the brain is akin to premature ageing of the cortex.” New research from Newcastle University, UK, in collaboration with the Federal University of Rio de Janeiro, investigated the way the human brain folds and how this ‘cortical folding’ changes with age.Linking the change in brain folding to the tension on the cerebral cortex — the outer layer of neural tissue in our brains — the team found that as we age, the tension on the cortex appears to decrease. This effect was more pronounced in individuals with Alzheimer’s disease.Publishing their findings today in the academic journal PNAS, the team say this new research sheds light on the underlying mechanisms which affect brain folding and could be used in the future to help diagnose brain diseases. Share on Twitter
Share on Facebook Share on Twitter LinkedIn “One crucial answer they’ve stumbled upon lies in the organism’s hidden physiology. It turns out that winning produces a surge in testosterone, and this rising level of testosterone increases an individual’s competitive ability, such as its persistence and confidence, and thus increasing the odds of future victories,” Cheng explained to PsyPost.“Surprisingly, there’s been much less work on the winner effect and testosterone changes in humans. So we thought it is important to study this. In particularly, we focused on studying what happens to the physiology of people who win prestige — a form of contest that is very prevalent in our species, perhaps more so than direct physical contests based on dominance (that are common in other animals).”“We looked at this in a college marching band community, a social context in which talent, expertise, and musical ability are likely very important to one’s social rank in the community,” Cheng said. “What we found converges with what has been shown in other species — winning a high prestige standing predicts a rise in testosterone.”The researchers examined changes in testosterone levels over a 2-month period in 177 marching band members, who were surveyed about who they considered to be the most successful, skilled, or respected members of their musical community.They found that men who were ranked as the top members of the marching band showed a rising testosterone profile over the following months. Men with low-prestige, on the other hand, showed a decline or little change in testosterone. This was true even after controlling for the potential effects of dominance-based status, social popularity, and friendship network dynamics.“Our social experiences — such as the experiences of winning in a variety of different contexts that make us feel respected, admired, and proud — have far-reaching effects on our psychology and biology. The effects of these kinds of experiences have significant effects on our motivation, morale, and future success,” Cheng told PsyPost.“We found these effects of status-dependent testosterone changes in men only. By contrast, women’s status appeared to be unrelated to their prestige in the community. More work is needed on understanding how women compete for status and the physiological substrates that underlie women’s competitive encounters.”“It’s fascinating to think that much of what happens in human social dynamics is actually not that different from that we see in other animals,” Cheng added. “Comparative work that aims to understand the ways in which we are similar to and different from other primates is a crucial current and future direction for scientists.”The study, “Prestige in a Large-Scale Social Group Predicts Longitudinal Changes in Testosterone“, was authored by Joey T. Cheng, Olga Kornienko, and Douglas A. Granger. Share Email Men who achieve a high standing are rewarded with a boost in testosterone, according to new research published online in the Journal of Personality and Social Psychology. The study found social prestige predicted longitudinal changes in testosterone among men in a university marching band.“We were fascinated with the so-called ‘winner effect’ that have been observed in many different species, from insects, fish, to non-human primates,” said Joey T. Cheng, the corresponding author of the study and an assistant psychology professor at University of Illinois at Urbana-Champaign.“The winner effect refers to how an animal that has won a fight or some kind of competition is more likely to go on winning in subsequent encounters. Biologists have known about this for a very long time and have been wrestling with trying to understand how the winner effect comes about. That is, how does a previous victory help an individual win again?” Pinterest
The Uganda Virus Research Institute in Entebbe confirmed the Ebola virus findings in patient samples. Among the dead are a healthcare worker and several members of the same family, and Ebola cases, including the fatal ones, have now reached 20, the agency said. The outbreak is centered in Kibaale district, in the western part of the country. Nine of the deaths occurred in a family from Nyanswiga village, the WHO said. Other fatalities include a clinical officer who treated a patient and the woman’s 4-month-old child. The outbreak area is about 136 miles west of Kampala, Uganda’s capital and second-largest city. Of the 20 patients, 2 are hospitalized in stable condition: a 38-year-old woman who cared for her sister—the clinical officer who died—and a 30-year-old woman who helped bury the index patient, according to the WHO. Both women were hospitalized on Jul 23 with fever, vomiting, diarrhea, and abdominal pain, but so far no bleeding that is often seen in viral hemorrhagic fever (VHF). Jul 30 AP story The Ebola virus is highly contagious, and infections carry a high fatality rate, ranging from about 50% to 90%. Initial symptoms include fever, headache, joint and muscle aches, sore throat, and weakness, followed by diarrhea, vomiting, and stomach pain, according to the US Centers for Disease Control and Prevention (CDC). Hallmarks of Ebola infection include internal and external bleeding, and there is no vaccine or specific treatment for the disease. Jul 30, 2012 (CIDRAP News) – An Ebola outbreak in Uganda that has killed 14 people has mobilized global efforts to contain the disease, the World Health Organization (WHO) said yesterday. CIDRAP’s comprehensive VHF overview The hospital in Kibaale has set up a temporary isolation ward for suspected, probable, and confirmed cases, and Doctors Without Borders is assisting with the set-up. Though the health ministry and Mulago Hospital in Kampala has helped staff the isolation center, the WHO said more workers are urgently needed. National VHF surveillance systems and rapid diagnostic capacity can limit the extent of disease outbreaks, and more efforts are needed to build and maintain VHF networks across Africa, the group concluded. Several species of bats were found in vacant houses and in several classrooms of the village schoolhouse that the girl attended, and testing the bats for Ebola virus is ongoing, according to the EID report. See also: The report said rapid detection, high clinical suspicion, and appropriate use of isolation by hospital staff probably limited the size of the outbreak in the girl’s case. The authors noted that the CDC Viral Special Pathogens Branch and the Uganda Virus Research Institute have established a permanent high-containment lab that can test for filoviruses and other causes of VHF in the country. The WHO said in a Twitter post today that one of the patients died at Mulago Hospital after transferring from the district hospital, but that no infections have occurred in Kampala. According to the Reuters report, the transferred patient who died there was a local health worker. Jul 30 Reuters story WHO and CDC experts are in Kibaale to assist with response activities, the WHO reported. Medical teams are identifying all contacts who may have been exposed to confirmed or suspected patients since Jul 6 for follow-up, and the groups are mobilizing supplies and logistics to help treat patients. The authors wrote that the girl’s exposure was probably zoonotic and occurred near her residence, given her relatives’ reports that the girl did not travel and that another family member had serologic evidence of infection that wasn’t related to the girl’s case. Jul 27 EID report The WHO said in its Twitter posts that Ebola outbreaks are normally very localized, and the risk of international spread is very small. It does not recommend any travel or trade restrictions. WHO Twitter feed Identification of the disease in many cases may have been delayed, because doctors initially thought the patients’ symptoms weren’t typical for Ebola, and some people put off medical care because they thought the infections were caused by “evil spirits,” Reuters reported. May 16, 2011, CIDRAP News Scan “Ugandan girl dies of Ebola fever” Uganda’s health ministry and its partners are finalizing national and district response plans, and the ministry has reactivated a national taskforce to address the Ebola outbreak. Meanwhile, a district task force in Kibaale has been formed and is coordinating the field response, as bordering districts raise their alert level and increase surveillance for new infections. A reporter from a local radio station said some of the hospital’s staff had fled the facility but are returning now that authorities have provided them with protective gear, Reuters reported today. The 2011 investigation into the girl’s death found evidence the Sudan Ebola subtype, which has been linked with large hemorrhagic fever outbreaks in Africa. Follow-up of 25 close contacts of the girl found no other infections, but blood tests on a juvenile relative found evidence of a past Ebola infection, which didn’t appear to be temporally related to the girl’s infection. Stephen Byaruhanga, health secretary of Kibaale district, told the Associate Press (AP) today that six more suspected patients have been admitted to the hospital, raising fears that the outbreak could involve more villages. The health ministry has urged the public to take precautions to curb the spread of the disease, and today Uganda’s president Yoweri Museveni issued a public statement urging people to avoid shaking hands, having casual sex, and participating in burials, according to the Reuters report. Jul 29 WHO statement Previous Uganda casesUganda’s last reported Ebola case occurred in May 2011, in a 12-year-old girl from Luwero district who died from the disease and whose illness and lab findings were described in a Jul 27 report in Emerging Infectious Diseases (EID) by CDC researchers and their partners in Uganda. Prior to that, a 2007 Ebola outbreak in Uganda killed 37 people. That outbreak was the first to involve the newly discovered Bundibugyo subtype. A 2000 Uganda outbreak involved 425 cases, 224 of them fatal.
Nov 21, 2012Fourth case of novel coronavirus infection reportedSaudi Arabia’s Ministry of Health this week confirmed the world’s fourth case of infection with a novel coronavirus first identified in September, the Saudi Gazette reported today. The Saudi native was admitted to a hospital in Riyadh but has improved after treatment, and tests at a reference lab outside the country were positive for the new coronavirus. Few other details were provided. The first reported case was fatal, while the second and third case-patients remain hospitalized in the United Kingdom and Saudi Arabia, respectively.Nov 21 Saudi Gazette storyECDC panel publishes airline trace-back guidance for viral hemorrhagic feversA European expert advisory panel recommends trace-back of airplane passengers only if Lassa, Ebola, or Marburg hemorrhagic fever is confirmed in an index patient and other criteria are met, the group reported in BMC Public Health today. The panel, commissioned by the European Centre for Disease Prevention and Control (ECDC), undertook a thorough review of the literature and consulted viral hemorrhagic disease (VHF) experts. Given that “no evidence of transmission of VHF during air travel exists to date,” the panel recommends trace-back investigations to begin only if: (1) the index case had symptoms during the flight, (2) the flight was within 21 days after pathogen detection, and (3) for Lassa fever, if exposure of body fluid has been reported. The panel recommends beginning trace-back only after confirmation of the index case and including only passengers and crew with direct contact, passengers who sat on either side of the index patient, and crew and cleaning personal of the index patient’s section of the aircraft.Nov 21 BMC Public Health abstractUS West Nile cases, deaths still risingThe US Centers for Disease Control and Prevention (CDC) said today that it received reports of 79 more West Nile virus (WNV) infections over the past week, raising the nation’s total for the year so far to 5,207. Five more deaths were reported, pushing that number to 234, according to the CDC’s update. The nation’s WNV activity is at the highest for the third week of November since 2003. New York was added to a list of states that make up 80% of the cases. The others are Texas, California, Louisiana, Illinois, Mississippi, Michigan, South Dakota, Oklahoma, Nebraska, Colorado, Arizona, Ohio, and New York.Nov 21 CDC WNV updateCDC details Salmonella outbreak in Lebanese tahiniA report of the first US outbreak of Salmonella serotype Bovismorbificans associated with tahini (sesame seed paste), an ingredient used in hummus and other Mediterranean-style foods, demonstrates the difficulty of tracing ingredient-driven outbreaks and emphasizes the importance of PulseNet in identifying disease clusters in geographically dispersed cases. The report, in the current Morbidity Mortality Weekly Report (MMWR), describes the identification and investigation of 23 culture-confirmed cases of Salmonella Bovismorbificans having indistinguishable pulsed-field gel electrophoresis (PFGE) patterns that occurred in seven states and the District of Columbia (DC) from September through November 2011. Many of the cases were identified through PulseNet, the national database of public health and food regulatory agency laboratories. In May 2012, trace-back investigation found that contaminated tahini used in hummus and perhaps other foods served at three Mediterranean-style restaurants in DC and northern Virginia was the probable source of the outbreak. The tahini came from a common manufacturer in Lebanon.Nov 23 MMWR report
A draft of a federal government risk study to assess contamination in spices found that about 12% of shipments were tainted with pathogens such as Salmonella or filth that included insect parts or animal hair.The detailed look at the cleanliness of the nation’s spice supply unveiled by the Food and Drug Administration (FDA) yesterday was prompted by a large Salmonella Rissen outbreak in the United States in 2008 and 2009 that sickened nearly 100 people in five states and was linked to ground white pepper.A few months later, a Salmonella Montevideo and Seftenberg outbreak linked to a cracked pepper coating on salami products sickened 272 people in 44 states.The United States imports most of its spices, except for dehydrated onions. About 86% of US households use spices, and usage has increased steadily since 1966, according to the report.The 213-page report, written by the FDA Center for Food Safety and Nutrition, details past outbreaks, results of federal and industry product sampling, mitigation strategies, and gaps in scientific knowledge.The FDA said the report is designed to assist with policy making decisions and help producers, importers, and other stakeholders. It said the draft of the report will be posted in the Federal Register, and it invited stakeholders and the public to comment on the findings.Salmonella most common pathogenThe FDA team identified 14 foodborne outbreaks linked to spices from 1973 to 2010, including five in the United States. In total, the events sickened 1,946 people and led to 128 hospitalizations and 2 deaths. Investigators noted that infants and children were the hardest-hit groups in five of the outbreaks.Ten of the outbreaks involved Salmonella enterica subtypes. Pepper spices—black, white, red, and unspecified—were implicated in nine of the outbreaks. Most of the spices were imported, which the FDA said isn’t surprising, because most of the countries reporting the outbreaks are not spice-producing countries.A review of import testing data found a 6.6% Salmonella prevalence in spice shipments, which is higher than other imported foods subject to the same FDA regulations and testing. More than 80 different Salmonella serotypes were found in the 3-year testing period that the FDA examined.The most common filth adulterants were insect parts, whole insects, and animal hair. Nearly all the insects found in the spices were those commonly found in stored item, which hints at problems with packing and storage, the agency said.FDA inspections in 2010 at 59 domestic facilities that pack and repack spices found that 10% had Salmonella in the environment, and problems with pest management was the most frequently cited observation.Common safety gapsSpices can become contaminated at several points along the production chain, the FDA said. In spice-producing countries, the items are often grown on small farms, then sold and combined with harvest from other farms. The spices are often held and dried in the open air, then sent to companies to be processed and packaged.Treatments to reduce contamination aren’t uniformly applied to all spices or all lots of a spice at a given time, the team found.Most safety gaps are basic, such as failing to limit animal access to spice sources during harvest or drying or failing to limit insect exposure during storage, the team said. “Based on our research, we concluded that knowledge and technology are available to significantly reduce the risk of illness from consumption of contaminated spices in the United States.”Future mitigation steps could include, for example, new enforcement and regulatory steps, education, and training, the investigators found.The FDA Food Safety Modernization Act of 2011 gives health officials new tools to boost the safety of spice shipments, including new recall authority and more frequent foreign and domestic inspections, according to the report. The authors also credited spice and food trade groups for developing recent guidance to control contamination.Federal Register comments can be submitted starting on Nov 4, the FDA said.See also:Oct 30 FDA draft risk profile on contamination in spicesOct 30 FDA press release on the reportFederal Register notice